SLC26A4-AS1 通过增强 SLC26A4 的表达加剧 AngII 诱导的心肌肥厚。
SLC26A4-AS1 Aggravates AngII-induced Cardiac Hypertrophy by Enhancing SLC26A4 Expression.
机构信息
Departamento de Cardiologia, Anhui Provincial Chest Hospital, (Instituto de Controle de Tuberculose de Anhui), Hefei, Anhui - China.
Departamento de Cardiologia, the Second People's Hospital of Hefei (Hospital Hefei afiliado à Medical University of Anhui), Hefei, Anhui - China.
出版信息
Arq Bras Cardiol. 2023 Apr 21;120(4):e20210933. doi: 10.36660/abc.20210933. eCollection 2023.
BACKGROUND
It has been reported that solute carrier family 26 members 4 antisense RNA 1 (SLC26A4-AS1) is highly related to cardiac hypertrophy.
OBJECTIVE
This research aims to investigate the role and specific mechanism of SLC26A4-AS1 in cardiac hypertrophy, providing a novel marker for cardiac hypertrophy treatment.
METHODS
Angiotensin II (AngII) was infused into neonatal mouse ventricular cardiomyocytes (NMVCs) to induce cardiac hypertrophy. Gene expression was detected by quantitative real-time PCR (RT-qPCR). Protein levels were evaluated via western blot. Functional assays analyzed the role of SLC26A4-AS1. The mechanism of SLC26A4-AS1 was assessed by RNA-binding protein immunoprecipitation (RIP), RNA pull-down, and luciferase reporter assays. The P value <0.05 was identified as statistical significance. Student's t-test evaluated the two-group comparison. The difference between different groups was analyzed by one-way analysis of variance (ANOVA).
RESULTS
SLC26A4-AS1 is upregulated in AngII-treated NMVCs and promotes AngII-induced cardiac hypertrophy. SLC26A4-AS1 regulates its nearby gene solute carrier family 26 members 4 (SLC26A4) via functioning as a competing endogenous RNA (ceRNA) to modulate the microRNA (miR)-301a-3p and miR-301b-3p in NMVCs. SLC26A4-AS1 promotes AngII-induced cardiac hypertrophy via upregulating SLC26A4 or sponging miR-301a-3p/miR-301b-3p.
CONCLUSION
SLC26A4-AS1 aggravates AngII-induced cardiac hypertrophy via sponging miR-301a-3p or miR-301b-3p to enhance SLC26A4 expression.
背景
已有报道称溶质载体家族 26 成员 4 反义 RNA 1（SLC26A4-AS1）与心肌肥厚高度相关。
目的
本研究旨在探讨 SLC26A4-AS1 在心肌肥厚中的作用及具体机制，为心肌肥厚的治疗提供新的标志物。
方法
采用血管紧张素Ⅱ（AngⅡ）诱导新生鼠心肌细胞（NMVCs）构建心肌肥厚模型，实时定量 PCR（RT-qPCR）检测基因表达，Western blot 检测蛋白水平，功能实验分析 SLC26A4-AS1 的作用，采用 RNA 结合蛋白免疫沉淀（RIP）、RNA 下拉和荧光素酶报告基因实验等方法评估 SLC26A4-AS1 的作用机制。P 值<0.05 为差异有统计学意义。采用 Student's t 检验进行两组比较，采用单因素方差分析（ANOVA）比较多组间差异。
结果
SLC26A4-AS1 在 AngⅡ处理的 NMVCs 中上调，并促进 AngⅡ诱导的心肌肥厚。SLC26A4-AS1 作为竞争性内源性 RNA（ceRNA）调节其附近基因溶质载体家族 26 成员 4（SLC26A4），在 NMVCs 中调节 microRNA（miR）-301a-3p 和 miR-301b-3p。SLC26A4-AS1 通过上调 SLC26A4 或海绵 miR-301a-3p/miR-301b-3p 促进 AngⅡ诱导的心肌肥厚。
结论
SLC26A4-AS1 通过海绵 miR-301a-3p 或 miR-301b-3p 增强 SLC26A4 的表达，加重 AngⅡ诱导的心肌肥厚。
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